Reports of Biochemistry and Molecular Biology

en Zinc Oxide Nanoparticles Ameliorate Histological Alterations Through Apoptotic Gene Regulation in Rat Model of Liver Ischemia-Reperfusion Injury زیست شناسی ملکولی Molecular Biology مقالات اصلی Original Article <div class="WordSection1"> <div style="text-align: justify;">Background: Organ ischemia-reperfusion (IR) is a common clinical condition associated with various situations such as trauma surgery, organ transplantation, and myocardial ischemia. Current therapeutic methods for IR injury have limitations, and nanotechnology, particularly zinc oxide nanoparticles (ZnO NPs), offers new approaches for disease diagnosis and treatment. In this study, we investigated the protective and anti-apoptotic effects of ZnO NPs in liver ischemia-reperfusion (IR) injury in rats. Methods: Forty-eight male rats were divided into six groups: sham, ZnO5, ZnO10, ischemia-reperfusion (IR), IR+ZnO5, and IR+ZnO10. The protective effect of ZnO NPs was evaluated by liver enzymes (AST, ALT, Bilirubin, ALP), biochemical (TAC, TNF-α, and MDA), molecular examinations (Bcl2, BAX), and histopathological evaluations (H&E, TUNEL). Results: Pre-treatment with ZnO5 and ZnO10 improved hepatic function in IR liver injury, attenuated the levels of oxidants (P = 0.03) and inflammatory mediators, and reduced apoptosis (P = 0). ZnO10 was found to have a greater effect on ischemic reperfusion injury than ZnO5 did. Histopathological examination also showed a dose-dependent decrease in alterations in the IR+ZnO5 and IR+ZnO10 groups. Conclusion: Administration of ZnO5 and ZnO10 improved liver function after IR. The findings of this study suggest that ZnO NPs have a protective effect against oxidative stress and apoptosis in liver ischemia-reperfusion injury in rats. These results may have important implications for developing advanced methods in ischemia-reperfusion treatment. Keywords: Anti Apoptotic Protein, Caspase 3, Metal Nanoparticle, Zinc Compounds.</div> <div align="center" style="text-align:center"> <hr align="center" noshade="noshade" size="2" style="color:#0f243e" width="100%" ></div> </div> <div style="text-align: justify;"><div aria-label="Page Break" class="cke_pagebreak" contenteditable="false" data-cke-display-name="pagebreak" data-cke-pagebreak="1" style="page-break-after:always" title="Page Break"></div></div> <div class="WordSection1"> <div style="text-align: justify;">Background: Organ ischemia-reperfusion (IR) is a common clinical condition associated with various situations such as trauma surgery, organ transplantation, and myocardial ischemia. Current therapeutic methods for IR injury have limitations, and nanotechnology, particularly zinc oxide nanoparticles (ZnO NPs), offers new approaches for disease diagnosis and treatment. In this study, we investigated the protective and anti-apoptotic effects of ZnO NPs in liver ischemia-reperfusion (IR) injury in rats. Methods: Forty-eight male rats were divided into six groups: sham, ZnO5, ZnO10, ischemia-reperfusion (IR), IR+ZnO5, and IR+ZnO10. The protective effect of ZnO NPs was evaluated by liver enzymes (AST, ALT, Bilirubin, ALP), biochemical (TAC, TNF-α, and MDA), molecular examinations (Bcl2, BAX), and histopathological evaluations (H&E, TUNEL). Results: Pre-treatment with ZnO5 and ZnO10 improved hepatic function in IR liver injury, attenuated the levels of oxidants (P = 0.03) and inflammatory mediators, and reduced apoptosis (P = 0). ZnO10 was found to have a greater effect on ischemic reperfusion injury than ZnO5 did. Histopathological examination also showed a dose-dependent decrease in alterations in the IR+ZnO5 and IR+ZnO10 groups. Conclusion: Administration of ZnO5 and ZnO10 improved liver function after IR. The findings of this study suggest that ZnO NPs have a protective effect against oxidative stress and apoptosis in liver ischemia-reperfusion injury in rats. These results may have important implications for developing advanced methods in ischemia-reperfusion treatment.</div> <div align="center" style="text-align:center"> <hr align="center" noshade="noshade" size="2" style="color:#0f243e" width="100%" ></div> </div> <div style="text-align: justify;"><div aria-label="Page Break" class="cke_pagebreak" contenteditable="false" data-cke-display-name="pagebreak" data-cke-pagebreak="1" style="page-break-after:always" title="Page Break"></div></div> Anti Apoptotic Protein, Caspase 3, Metal Nanoparticle, Zinc Compounds. 619 630 http://rbmb.net/browse.php?a_code=A-10-1171-2&slc_lang=en&sid=1 Maryam Jafar Sameri 100319475328460020245 100319475328460020245 No Department of physiology, medicine faculty, Abadan University of Medical Sciences, Abadan, Iran. Feryal Savari savari.f@ajums.ac.ir 100319475328460020246 100319475328460020246 Yes Department of Medical Basic Sciences, Shoushtar Faculty of Medical Sciences, Shoushtar, Iran. Seyyed Ali Mard 100319475328460020247 100319475328460020247 No Clinical Sciences Research Institute, Alimentary Tract Research Center, Department of Physiology, The School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Anahita Rezaie 100319475328460020248 100319475328460020248 No Department of Pathobiology, School of Veterinary Medicine, Shahid Chamran University of Ahvaz, Ahvaz, Iran. Mojtaba Kalantar 100319475328460020249 100319475328460020249 No Department of Occupational Health, Shoushtar Faculty of Medical Sciences, Shoushtar, Iran.